As used herein, the term tachycardia refers to any fast abnormal rhythm of the heart that is amenable to treatment by electrical discharges and specifically includes supraventricular tachycardia (SVT), atrial tachycardia (AT), atrial fibrillation and atrial flutter (AF), ventricular tachycardia (VT), and ventricular flutter and ventricular fibrillation (VF).
U.S. Pat. No. 3,857,398 to Rubin, dated Dec. 31, 1974, and entitled "Electrical Cardiac Defibrillator," describes a combined pacer/defibrillator. This device either performs a bradycardia pacing or a defibrillation function depending on the detection of a VT/VF. If a VT/VF is detected, the device is switched to the defibrillating mode. After a period of time to charge the capacitor, a defibrillation shock is delivered to the patient.
Improvements on this device were contained in a multiprogrammable, telemetric, implantable defibrillator which is disclosed in copending patent application Ser. No. 239,624 to Gilli et al., filed Sep. 1, 1988, and entitled "Reconfirmation Prior to Shock in Implantable Defibrillator". The Gilli et al. device contains a bradycardia support system as well as a high energy shock system to revert ventricular tachycardias to normal sinus rhythm. On reconfirmation of the presence of a tachycardia, a shock is delivered to the patient at a predetermined time or when the desired energy level is reached.
As cardioversion or defibrillation shocks can be very unpleasant to a patient, especially when delivered frequently, it became necessary therefore to provide a device which included antitachycardia pacing therapy along with bradycardia support pacing therapy and defibrillation or cardioversion therapy, so that the implanted device could automatically provide the necessary therapy from a range of therapies offered by the device. Hence a further development in the field of combined implantable devices is described in U.S. Pat. No. 4,940,054, to Grevis and Gilli, dated Jul. 10, 1990, and entitled "Apparatus and Method for Controlling Multiple Sensitivities in Arrhythmia Control Systems Including Post Therapy Pacing Delay". This device is a microcomputer based arrhythmia control system which is programmable by means of a telemetric link. The device provides single chamber bradycardia support pacing, antitachycardia pacing, and cardioversion or defibrillation shocks for restoring normal sinus rhythm to a patient.
Additionally, various specific developments have been made in the field of tachycardia control pacers. Tachycardia is a condition in which the heart beats very rapidly, with a ventricular rate higher than 100 beats per minute (bpm) and typically above 150 bpm, and an atrial rate as high as 400 bpm. There are several different pacing modalities which have been suggested for the termination of tachycardia. The underlying principle in all of them is that if a pacer stimulates the heart at least once shortly after a heartbeat, before the next naturally occurring heartbeat at the rapid rate, the heart may successfully revert to normal sinus rhythm. Tachycardia is often the result of electrical feedback within the heart. A natural beat results in the feedback of an electrical stimulus which prematurely triggers another beat. By interposing a stimulated heartbeat, the stability of the feedback loop is disrupted.
U.S. Pat. No. 4,202,340, to Langer et al., dated May 13, 1980, and entitled "Method and Apparatus for Monitoring Heart Activity, Detecting Abnormalities, and Cardioverting a Malfunctioning Heart," describes an antitachycardia pacing system which detects VT/VF by deriving a probability density function from the analysis of the amplitudes of intracardiac signals. This antitachycardia pacing system is subject to errors in the delivery of therapy due to the erratic and unpredictable nature of intracardiac signals.
The system disclosed in U.S. Pat. No. 4,475,551, to Langer et al., dated Oct. 9, 1984, and entitled "Arrhythmia Detection and Defibrillation System and Method," illustrates arrhythmia detection in which the device first analyzes the probability density function to ascertain abnormal cardiac rhythms such as fibrillation, high rate tachycardias, and low rate tachycardias. Upon the discovery of such rhythms, the device senses heart rate so as to distinguish fibrillation and high rate tachycardia from low rate tachycardia. This device employs a predetermined threshold value for the rate which distinguishes such arrhythmia events.
U.S. Pat. No. 4,291,699, to Geddes, dated Sep. 29, 1981, and entitled "Method and Apparatus for Automatically Detecting and Treating Ventricular Fibrillation," characterizes a defibrillator which senses both the electrical and mechanical activity of the heart to detect fibrillation. This device measures the mechanical pumping action of the heart by detecting changes in electrical impedance between a pair of electrodes implanted within one of the ventricles of the heart.
Dual chamber heart pacers have been developed in order to generate sequential atrial and ventricular pacing pulses which closely match the physiological requirements of the patient. A conventional dual chamber heart pacer as disclosed in U.S. Pat. No. 4,429,697 to Nappholz et al. dated Feb. 7, 1984, and entitled "Dual Chamber Heart Pacer With Improved Ventricular Rate Control," includes atrial beat sensing and pulse generating circuits along with ventricular beat sensing and pulse generating circuits. It is known that the detection of a ventricular beat or the generation of a ventricular pacing pulse initiates the timing of an interval known as the V-A delay. If an atrial beat is not sensed prior to expiration of the V-A delay interval, then an atrial pacing pulse is generated. Following the generation of an atrial pacing pulse, or a sensed atrial beat, an interval known as the A-V delay is timed. If a ventricular beat is not sensed prior to the expiration of the A-V delay interval, then a ventricular pacing pulse is generated. With the generation of a ventricular pacing pulse, or the sensing of a ventricular beat, the V-A delay timing starts again. This patent describes how the V-A delay timing interval may be divided into three parts; the atrial refractory period, the Wenckeback timing window, and the P-wave synchrony timing window. It outlines the importance of controlling the ventricular rate in comparison with the atrial rate in order to maintain synchrony between the atrium and the ventricle. The patent does not however address the issue of antitachycardia pacing therapy.
Physiological pacers adapt pacing rate and timing to the patient's needs based on one of two general schemes: dual-chamber pacing in which intrinsic atrial activity triggers ventricular pacing, and pacing (single-chamber or dual-chamber) at a ventricular rate related to metabolic demand which is sensed in some manner. Each method of rate adaptation has inherent advantages and disadvantages which a physician must consider in determining the best method for pacing within a diverse patient population.
Dual-chamber pacemakers perform rate adaptation by means of atrial synchronous ventricular pacing where sensing of a natural atrial pulse, called a P wave, activates the process leading to ventricular demand pacing by starting the timing period called the A-V interval. During the A-V interval, the ventricular sense amplifier is capable of sensing a naturally occurring ventricular contraction, or R wave. If the pacer senses an R wave during the A-V interval, a second time period called the V-A interval is immediately started, at the end of which an atrial pulse is generated. If the A-V interval times out before R wave sensing, however, the pacemaker stimulates the ventricle and the V-A interval begins at the end of the A-V interval. This operating mode, characterized by pacing, sensing, and inhibition in both chambers is termed a DDD mode. Atrial synchronous ventricular pacing is best for patients and conditions in which the sino-atrial node is normally responsive to metabolic demands since intrinsic stimulation by the sinus node appropriately controls cardiac rate. Pacing in a dual-chamber manner promotes efficient cardiac output by pacing at a natural rate and by maintaining physiological A-V synchrony. DDD pacing is ineffective where an electrically unstable atrium produces frequent extra-systoles, creating intermittent atrial flutter or fibrillation.
Metabolic demand pacemakers, on the other hand, perform rate adaptation using various sensors within the body to measure a parameter related to metabolic demand and to determine a desired pacing rate independent of atrial activity. Recent pacemaker technological advances include a number of accurate physiological sensor mechanisms for determining pacing rate in response to metabolic needs of the body. These metabolic demand pacemakers have clinically proven themselves to properly support the patient's needs. The pacemaker measures a metabolic sensor parameter and, from the parameter, determines a metabolic indicator rate (MIR). In one example of a metabolic demand indicator scheme, U.S. Pat. No. 4,901,725, dated Feb. 20, 1990 to Nappholz et al., entitled "Minute Volume Rate-Responsive Pacemaker," changes in minute ventilation, measured using transthoracic impedance, correlate positively to heart rate. Updating cardiac rate relative to the minute ventilation measurement increases pacing rate in a stable but rapid manner, proportional to the level of the workload. Because such pacers do not directly trigger ventricular pacing upon atrial sensing, it follows that these pacemakers do not drive the ventricle in response to unstable upper atrial rate behavior or induce pacemaker mediated tachycardia. However, these pacers do not provide the hemodynamic efficiency inherent in A-V synchronous pacing; in many metabolic pacemakers, the sensor mechanism responds to changing metabolic demand more slowly than a system driven by the sinus node. Also, because a metabolic sensor measures a parameter only secondarily related to cardiac function, extrinsic influences on the sensor may change the heart rate inappropriately.
Prior art single chamber antitachycardia pacing devices which provide antitachycardia pacing bursts to either the atrium or the ventricle have shortcomings in that they lack the required synchrony between the atrium and the ventricle. This reduces the percentage of successful reversions, especially in the case of ventricular antitachycardia pacing. Although such pacing may revert an arrhythmia, at the same time however, it increases the risk of adversely affecting the patient by means of a decrease in arterial pressure due to the rapid pacing. Possibly, as a result of the hemodynamic compromise or lowered hemodynamic status of the myocardium during the arrhythmia and pacing which reduces electrical conduction in the heart, there is a high risk of a ventricular tachycardia accelerating to a faster ventricular tachycardia and even to a ventricular fibrillation. This has been shown in an article by Fisher et al. entitled "Termination of Ventricular Tachycardia with Burst or Rapid Ventricular Pacing", American Journal of Cardiology, Vol. 41 (January, 1978), page 96. Not only does this present a potentially hazardous situation to the patient, but it also makes it more difficult for the device to revert the patient. Reversion would necessarily demand more energy of the device and perhaps even cardioversion or defibrillation therapy which is not available in many pacing devices. Furthermore, prior art devices are very limited in the provision of individualized therapy to the patient by patient dependent parameters such as the A-V delay.
Many antitachycardia pacing therapy devices at present include defibrillation support within the device in order to provide adequate safety to a patient. It is highly advantageous to prevent the development of VT's or atrial fibrillations, or to terminate them quickly if they appear, rather than allowing the arrhythmia to develop to such an extent that a defibrillation shock is necessary.
The use of antitachycardia pacing therapy in conjunction with a dual chamber pacing device is disclosed in the copending application of Norma L. Gilli, Ser. No. 462,499, filed Jan. 5, 1990, and entitled "Apparatus and Method for Antitachycardia Pacing in Dual Chamber Arrhythmia Control System", which application is assigned to the assignee of the present invention. In the Gilli application upon detection of the presence of a tachycardia, the tachycardia cycle length (TCL) is measured and a V-A interval less than or equal to the TCL is determined, along with an initial value A-V interval. Stimulation pulses are then delivered until the expiration of a given number (N) V-A intervals and N A-V intervals to complete a first train of pulses. A series of a given number (M) of trains of pulses similar to the first train of pulses is delivered, and the A-V delay interval value is varied from the initial value thereof at least once prior to the completion of the series of M trains of pulses. Monitoring of intrinsic QRS complexes between pulse trains is performed. If the tachyarrhythmia is deemed to be accelerating, one of cardioversion or defibrillation is employed. The present invention is an improvement over said Gilli application with respect to the manner of detecting tachyarrhythmias and the manner of setting the A-V interval during the application of antitachycardia pacing therapy.